Pathogenic Mechanisms of P. aeruginosa Keratitis: A Review of the Role of T Cells,Langerhans Cells,PMN,and Cytokines

The aim of this article is to review our current understanding of the role of cytokines, chemokines, T cells, Langerhans cells, and neutrophils (PMN) and their interactions in vivo in the host response to Pseudomonas aeruginosa ocular challenge. The cellular/cytokine network in vivo has begun to be unraveled, and the data discussed provide substantive evidence for a regulatory role of CD4⁺ T cells (Th1 type) contributing directly to persistence of PMN in the cornea of susceptible C57BL/6 (cornea perforates) versus resistant BALB/c (cornea heals) mice. Additionally, in the susceptible mouse model, CD4⁺ T cells interact with Langerhans cells and B7/CD28 ligation appears critical for antigen presentation and the susceptibility response. Various cytokines and chemokines (e.g., MIP-1α, IL-1β, MIP-2, IL-12, and IFN-γ) and their pattern of sustained upregulation after infection in susceptible versus resistant mice also will be discussed in light of an in vivo cytokine network. T-cell-mediated pathogenic mechanisms are of importance in development of the susceptible response to P. aeruginosa ocular infection. In the absence of T-cell infiltration into the cornea, PMN do not persist in the stroma, and cytokines and chemokines are better balanced, resulting in decreased stromal destruction and the resistance response.